Maternal periodontal disease and risk of preeclampsia: a meta-analysis.

Research on the association between maternal periodontal disease and the risk of preeclampsia has generated inconsistent results. This meta-analysis was conducted to evaluate the association between maternal periodontal disease and the risk of preeclampsia. A literature search of PubMed and Embase was performed to identify relevant papers published before March 2013. Only observational studies that assessed maternal periodontal disease and the risk of preeclampsia were selected. Patients' periodontal status was examined at different time points during pregnancy or after delivery (at 14-32 weeks of gestation, within 48 h prior to or within 5 days after delivery). Pooled odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated for cases and controls. Cases were defined as women with concurrent hypertension and proteinuria after 20 weeks of gestation. Eleven studies involving 1118 women with preeclampsia and 2798 women without preeclampsia were identified and analyzed. Women with periodontal disease before 32 weeks of gestation had a 3.69-fold higher risk of developing preeclampsia than their counterparts without periodontal disease (OR=3.69; 95% CI=2.58-5.27). Periodontal disease within 48 h prior to delivery was associated with a 2.68-fold higher risk of preeclampsia (OR=2.68; 95% CI=1.39-5.18). Pregnant women with periodontal disease within 5 days after delivery had a 2.22-fold higher risk of preeclampsia than women without periodontal disease (OR=2.22; 95% CI=1.16-4.27). In conclusion, this meta-analysis suggests that maternal periodontal disease is an independent predictor of preeclampsia.

Atypical imaging observations of branchial cleft cysts.

The aim of the present study was to assess the atypical imaging manifestations of branchial cleft cysts (BCCs) confirmed by pathology. Computerized tomography (CT) or magnetic resonance imaging (MRI) of 17 BCC cases were reviewed. The imaging features, including laterality, location, border, attenuation and internal architecture, were evaluated. All 17 cases were second BCCs, including 5 cases of Bailey type I classification cysts and 12 cases of type II classification cysts. The atypical imaging features included signal and morphological abnormalities. The abnormal signal intensities were caused by intracapsular bleeding (n=2) or solidification of cystic fluid (n=2). Intracystic hemorrhaging revealed homogeneous hyperintensity on T1-weighted image (T1WI) and T2-weighted image (T2WI). Solidification of cystic fluid revealed slightly homogeneous hyperintensity compared with muscle on T1WI and homogeneous hypointensity on T2WI without enhancement. The aberrant morphology mainly presented as thickening of the cystic wall (n=13). Thickened walls of BCCs with ill- (n=5) or well- (n=8) defined borders were observed in 13 patients. In 3 patients, significant enhancement was identified following intravenous gadolinium administration (n=4). When with atypical CT or MRI features are presented, the typical location of BCCs can help in the diagnosis, as it is located at the lateral portion of the neck adjacent to the anterior border of the mandibular angle or sternocleidomastoid muscle. The atypical observations, including variable signals, imply that the cystic content has changed. Thickened walls indicate inflammation or cancerous tendency and patients with ill-defined margins, vascular involvement or lymphadenopathy atelectasis indicate malignant conversion.